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"EBV causes typically an asymptomatic infection or can cause acute tonsillitis as a part of bigger infection called infectious mononucleosis also known as glandular fever. EBV typically occurs in adolescents and young adults and is transmitted orally via saliva. This is the reason EBV infections are also known as the kissing disease. Nearly everyone will become infected with EBV at some point, the good thing is for most of us it is asymptomatic. In this videos we will talk about a primary EBV infection which is asymptomatic and how the infection can evolve to be become infectious mononucleosis which is a symptomatic condition.
The pathophysiology of EBV infection begin with saliva transmission and the EBV virus targeting the tonsils which is a lymphoid tissue made up of T cells and B cells. In the tonsil the EBV target B cells and tonsillar epithelial cells. This is called the EBV primary infection and is usually asymptomatic. Once EBV infects the B cells the EBV has an Incubation period of about 2-6 weeks. During the incubation period a number of things happen:
EBV replicates in B-cell and the virus is shed intermittently into pharyngeal secretions, particularly saliva. Saliva is therefore how EBV is transmitted between people.
The cycle can continue and the person can be completely asymptomatic of course during this incubation and reactivation time the immune system will respond.
EBV Induces an immune response where by b cells capture an antigen of EBV and processes it, The b-cells can mount an immune response locally in the tonsils and the B cells enter circulation and mount an immune response in the lymph node, spleen and liver. Here the B cells stimulate CD8 T cell activity. CD8 t cells also known as cytotoxic t cells are important in the suppression of primary EBV infection. On a side note the CD8+ are thought to be the important players in preventing EBV reactivation and EBV associated lymphoproliferative disease. The B cells also activate CD4+ T cells through costimulation, which means the B cells also become activated. Activated B cells become plasma cells. The plasma cells are the antibody producing cells. The plasma cells will produce EBV specific antibodies which mean antibodies against components of the EBV - firstly the viral capsid antigen with IgM followed by the viral capsid antigen with igG. Plasma cells then eventually produce epstein Barr nuclear antigen igG once infection is resolved. The activation of other immune cells in the lymph nodes, spleen and liver is part of the immune response against EBV.
During the incubation period the EBV can also enter circulation. Here the immune cells in the blood will try to destroy them and also mount an immune response releasing cytokines. This interaction is one of the reasons why people in EBV infection become febrile and feel miserable.
During the incubation period the abnormal infiltrated B cells produce heterophile antibodies which is an important and quick marker for diagnosing EBV"
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Great info, thanks..
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A small request ..... can you make more videos on herpes virus family (herpes simplex; Varicella Zoster and Cytomegalovirus)
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does this infection impact the way my body responses to COVID-19?
Only later on they did blood work and much later more proper blood work and I had antibodies but also found out I had hepetitis infection on top..
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does this infection impact the way my body responses to COVID-19?
Only later on they did blood work and much later more proper blood work and I had antibodies but also found out I had hepetitis infection on top..
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...That I made a month ago
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When I was 4 yrs old, I had acute tonsillitis and had my it sinks removed. Now as an adult, I have ms, with a low CD8 T cell blood count and an elevated CD4/CD8 ratio. Do I have a lot of CD8 cells sequestered in my CNS doing the damage and that's why they appear low in my peripheral blood? Or do I genetically not reduce enough CD8 cells and that's why my body is unable to fight the EBV, hence the ms? Thank you.
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